339.1 ð é«åžçç
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339.1.0.1.1 Nephrotic Syndrome
339.1.0.1.1.1 Definition (Classic Pentad)
- Proteinuria > 3.5 g/24 h (or UPCR > 3.5 or UACR > 2200 mg/g)
- Hypoalbuminemia (< 3.5 g/dL, often < 2.5)
- Edema (peripheral, periorbital, anasarca; pleural effusion, ascites)
- Hyperlipidemia (â LDL, TG)
- ± Hypercoagulability (loss of antithrombin III; â thrombosis especially renal vein)
339.1.0.1.1.2 Pathophysiology
- Glomerular basement membrane / podocyte injury
- Increased permeability to protein
- Albumin loss â low oncotic pressure â edema + compensatory hepatic lipoprotein synthesis
- Loss of immunoglobulins â â infection risk
- Loss of vitamin D-binding protein â vitamin D deficiency
- Loss of thyroxine-binding globulin â hypothyroidism (sometimes)
339.1.0.1.1.3 Common Causes
Primary (Idiopathic) â More Common in Adults: - Minimal Change Disease (MCD): most common in children (80%); ~ 10-20% adults - Focal Segmental Glomerulosclerosis (FSGS): most common cause of NS in adults in US - Membranous Nephropathy (MN): most common in older adults; anti-PLA2R, anti-THSD7A, anti-NELL-1 - Membranoproliferative GN (MPGN) / C3 glomerulopathy (C3G): complement-mediated - IgA Nephropathy (some can have nephrotic features)
Secondary: - Diabetic Kidney Disease (DKD) â most common cause of NS globally - Amyloidosis (AL, AA, hereditary) - Light chain deposition disease (MM-related) - Hepatitis B (MN) - Hepatitis C (MPGN, mixed cryoglobulinemia) - HIV (HIVAN â FSGS variant) - Drugs: NSAIDs, lithium, gold, penicillamine, ICI - Cancer: MN (paraneoplastic), AL - Pregnancy: preeclampsia, lupus - Sjögren, RA, sarcoidosis
339.1.0.1.1.4 Complications
- Thromboembolism (renal vein, DVT, PE)
- Infections (encapsulated organisms â S. pneumoniae)
- Edema (severe, anasarca)
- Hyperlipidemia + atherosclerosis
- Acute kidney injury (intravascular volume depletion, drug toxicity, RVT)
- Vitamin D deficiency
- Hypothyroidism (rare)
- Iron deficiency
339.1.0.1.2 Nephritic Syndrome
339.1.0.1.2.1 Definition
- Hematuria (dysmorphic RBC + RBC casts)
- Hypertension
- Edema (mild-moderate)
- AKI variable (rising Cr, oliguria possible)
- Proteinuria variable (sub-nephrotic typically; can be nephrotic in some)
- ± Constitutional symptoms (fever, malaise, joint pain)
339.1.0.1.2.2 Pathophysiology
- Glomerular inflammation (proliferative)
- Endothelial damage
- â GFR (acutely)
- Hematuria from disrupted GBM
- Activated complement (often)
339.1.0.1.2.3 Common Causes
Primary: - IgA Nephropathy â most common globally - Post-Infectious GN (PSGN) â strep, staph, others; classic in pediatric - MPGN / C3G â primary or secondary
Secondary (Common): - Lupus nephritis (Class I-VI; ISN/RPS 2003) - ANCA-associated vasculitis (GPA, MPA, EGPA) - Anti-GBM disease (Goodpasture) - Cryoglobulinemic vasculitis (often hep C-associated) - IgA vasculitis (Henoch-Schönlein purpura) - Post-infectious (other than strep â hep B, hep C, HIV, endocarditis) - MPGN (lupus, hep C, monoclonal gammopathy)
339.1.0.1.2.4 Rapidly Progressive GN (RPGN)
- Subset of nephritic with rapid decline
- Cr doubles in days-weeks
- Histology: crescents on biopsy
- 3 types (Couser classification):
- Anti-GBM (Type I) â Goodpasture
- Immune Complex (Type II) â lupus, post-infectious, IgA
- Pauci-Immune (Type III) â ANCA-associated
- Emergency: high-dose steroids + cyclophosphamide ± plasmapheresis
339.1.0.1.3 Diagnostic Workup
339.1.0.1.3.1 Initial Tests
- Urinalysis with microscopy
- UACR or UPCR (spot)
- 24-hour urine protein quantification
- Serum chemistry: Cr, BUN, electrolytes, glucose, albumin
- Lipid profile: nephrotic-range cholesterol + TG
- CBC + differential
- LFTs
339.1.0.1.3.2 Immunology Panel
- ANA, dsDNA: lupus
- Complement C3, C4: low in lupus, post-infectious GN, MPGN, C3G, cryoglobulin
- ANCA: GPA, MPA, EGPA
- Anti-GBM: Goodpasture
- Anti-PLA2R: primary MN (70-80%)
- Anti-THSD7A, anti-NELL-1: less common MN antibodies
- Anti-streptolysin O (ASO), anti-DNase B: PSGN
- RF, anti-CCP: RA
- Cryoglobulins: hepatitis C, lupus
- Hep B surface antigen, hep C antibody: hepatitis
- HIV: HIVAN
- Free light chains + SPEP/UPEP: myeloma, amyloid
- Complement C5b-9 (MAC), factor B: complement-mediated
339.1.0.1.3.3 Infectious Workup
- Blood cultures: endocarditis-associated
- Throat / skin cultures: PSGN
- Tuberculosis: secondary causes
339.1.0.1.3.4 Imaging
- Renal ultrasound: size, hydronephrosis, masses, cortical thinning
- CT: malignancy, vascular
- Doppler: renal vein thrombosis suspicion
339.1.0.1.3.5 Renal Biopsy (Gold Standard)
- For definitive diagnosis
- Light microscopy + immunofluorescence + electron microscopy
- Indications:
- Unexplained AKI
- Nephritic syndrome
- Nephrotic syndrome in adults (often)
- Rapidly progressive disease
- Steroid-resistant
- Complications: bleeding (1-2%), AV fistula
339.1.0.1.4 General Treatment Principles
339.1.0.1.4.1 Specific Therapy (Ch339)
- Tailored to specific GN
- Immunosuppression: steroids, cyclophosphamide, rituximab, MMF, CNIs, IS
339.1.0.1.4.2 Supportive Care
- ACE/ARB: reduce proteinuria + BP
- Dietary salt restriction
- Diuretics: loop ± thiazide; carefully (volume depletion + AKI)
- Statins: dyslipidemia, CV risk
- Anticoagulation: prophylactic for high-risk nephrotic (especially MN with severe hypoalbuminemia or large protein loss); LMWH or DOAC
339.1.0.2 𩺠åºé鿥
- Nephrotic: > 3.5 g/24h protein + hypoalbuminemia + edema + hyperlipidemia ± thrombosis
- Nephritic: hematuria + RBC casts + HTN + AKI variable
- Top nephrotic causes: MCD (kids), FSGS, MN (adults), DKD, amyloid
- Top nephritic causes: IgA, PSGN, lupus, ANCA, anti-GBM, MPGN/C3G
- RPGN 3 types: anti-GBM, immune complex, pauci-immune (ANCA)
- Workup: UA + UACR + immunology + biopsy
- Anti-PLA2R: primary MN (70-80%)
- C3 low: PSGN, lupus, MPGN, C3G, cryoglobulin